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Transcript
VIRAL HEPATITIS
Dr. Sh. Sali
Type of Hepatitis
A
Source of
virus
Route of
transmission
Chronic
infection
Prevention
B
C
D
E
feces
blood/
blood/
blood/
blood-derived blood-derived blood-derived
body fluids body fluids
body fluids
feces
fecal-oral
percutaneous percutaneous percutaneous
permucosal permucosal permucosal
fecal-oral
no
yes
yes
yes
no
pre/postpre/postblood donor
pre/postensure safe
exposure
exposure
screening;
exposure
drinking
immunization immunization risk behavior immunization;
water
modification risk behavior
modification
Hepatitis A

Hepatitis A, caused by infection with the hepatitis A virus
(HAV).

has an incubation period of approximately 28 days (range:
15–50 days).

HAV replicates in the liver and is shed in high concentrations
in feces from 2 weeks before to 1 week after the onset of
clinical illness.

HAV infection produces a self-limited disease that does not
result in chronic infection or chronic liver disease.

However, 10%–15% of patients might experience a relapse of
symptoms during the 6 months after acute illness.

Acute liver failure from hepatitis A is rare (overall case-fatality
rate: 0.5%).



The risk for symptomatic infection is directly related to age,
with >80% of adults having symptoms compatible with
acute viral hepatitis and the majority of children having
either asymptomatic or unrecognized infection.
Antibody produced in response to HAV infection persists for
life and confers protection against re-infection.
How is HAV transmitted?





Person-to-person transmission through the fecal-oral
route (i.e., ingestion of something that has been
contaminated with the feces of an infected person) is the
primary means of HAV transmission in the United States. Most
infections result from close personal contact with an infected
household member or sex partner.
Common-source outbreaks and sporadic cases also can occur
from exposure to fecally contaminated food or water.
Uncooked HAV-contaminated foods have been recognized as
a source of outbreaks.
Cooked foods also can transmit HAV if the temperature during
food preparation is inadequate to kill the virus or if food is
contaminated after cooking, as occurs in outbreaks associated
with infected food handlers.
Waterborne outbreaks are infrequent in developed countries
with well-maintained sanitation and water supplies.
Who is at increased risk for
acquiring HAV infection?




Travelers to countries with high or
intermediate endemicity of HAV
infection
Users of injection and non-injection
illegal drugs
Persons with clotting factor disorders
Persons working with nonhuman
primates susceptible to HAV infection
Signs & Symptoms










Some persons, particularly young children, are asymptomatic.
When symptoms are present, they usually occur abruptly and can
include the following:
Fever
Fatigue
Loss of appetite
Nausea
Vomiting
Abdominal pain
Dark urine
Clay-colored bowel movements
Joint pain
Jaundice .
When symptoms occur, how long do they usually last?
Symptoms usually last less than 2 months, although 10%–15%
of symptomatic persons have prolonged or relapsing disease for
up to 6 months.
Typical Serological
Course
Total antiHAV
Symptoms
Titr
e
ALT
Fecal
HAV
0
1
IgM anti-HAV
2
3
4
5
Months after
6
12
24
How long does HAV survive outside the body?
How can the virus be killed?




HAV can live outside the body for months,
depending on the environmental
conditions.
The virus is killed by heating to 185
degrees F (85 degrees C) for one minute.
However, the virus can still be spread
from cooked food if it is contaminated
after cooking.
Adequate chlorination of water, as
recommended in the United States, kills
HAV that enters the water supply.
Cont.


Can hepatitis A become chronic?
No. Hepatitis A does not become chronic.
Can persons become reinfected with
HAV after recovering from hepatitis
A?
No. IgG antibodies to HAV, which appear
early in the course of infection, provide
lifelong protection against the disease.
How is HAV infection prevented?





Vaccination with the full, two-dose series of hepatitis A
vaccine is the best way to prevent HAV infection.
Hepatitis A vaccine has been licensed in the United States
for use in persons 12 months of age and older.
The vaccine is recommended for persons who are more
likely to get HAV infection or are more likely to get
seriously ill if they get hepatitis A
Immune globulin is available for short-term protection
(approximately 3 months) against hepatitis A, both preand post-exposure. Immune globulin must be administered
within 2 weeks after exposure for maximum protection.
Good hygiene — including hand-washing or use of hand
sanitizer after using the bathroom, changing diapers, and
before preparing or eating food — is also integral to
hepatitis A prevention, given that the virus is transmitted
through the fecal–oral route.
Who should be vaccinated
against hepatitis A?






All children at age 1 year (i.e., 12–23
months). Children who have not been vaccinated by age
2 can be vaccinated at subsequent visits.
Children and adolescents ages 2–18 who live in
states or communities where routine hepatitis A
vaccination has been implemented because of high
disease incidence.
Persons traveling to or working in countries that
have high or intermediate rates of hepatitis A.
Persons who have occupational risk for infection
Persons who have chronic liver disease.
Persons who have clotting-factor disorders
Hepatitis A Vaccine




How long does protection from hepatitis A vaccine last?
At least 25 years in adults and at least 14–20 years in children.
Can hepatitis A vaccine be administered concurrently with other
vaccines?
Yes. Hepatitis B, diphtheria, poliovirus (oral and inactivated), tetanus,
oral typhoid, cholera, Japanese encephalitis, rabies, and yellow fever
vaccines and immune globulin can be given at the same time that
hepatitis A vaccine is given, but at a different injection site.
Can hepatitis A vaccine be given during pregnancy?
The safety of hepatitis A vaccination during pregnancy has not been
determined; however, because the vaccine is produced from
inactivated HAV, the theoretical risk to the developing fetus is
expected to be low.
Can hepatitis A vaccine be given to immunocompromised persons
(e.g., persons on hemodialysis or persons with AIDS)?
Yes. Because hepatitis A vaccine is inactivated.
Hepatitis B

Hepatitis B is a disease caused by hepatitis B virus which
infects the liver of hominoidae, including humans, and
causes an inflammation called hepatitis. Originally known as
"serum hepatitis",

The disease has caused epidemics in parts of Asia and
Africa, and it is endemic in China.

About a third of the world's population, more than 2 billion
people, have been infected with the hepatitis B virus.

This includes 350 million chronic carriers of the virus.

Transmission of hepatitis B virus results from exposure to
infectious blood or body fluids containing blood.


The acute illness causes liver
inflammation, vomiting, jaundice and—
rarely—death. Chronic hepatitis B may
eventually cause liver cirrhosis and liver
cancer—a fatal disease with very poor
response to current chemotherapy.
The infection is preventable by
vaccination.




Hepatitis B virus is an hepadnavirus—hepa from
hepatotrophic and dna because it is a DNA virus—and it has
a circular genome composed of partially double-stranded
DNA.
The viruses replicate through an RNA intermediate form by
reverse transcription, and in this respect they are similar to
retroviruses.
Although replication takes place in the liver, the virus
spreads to the blood where virus-specific proteins and their
corresponding antibodies are found in infected people.
Bloods test for these proteins and antibodies are used to
diagnose the infection.
Transmission





Transmission of hepatitis B virus results from exposure to
infectious blood or body fluids containing blood.
Possible forms of transmission include (but are not limited
to) unprotected sexual contact, blood transfusions, re-use
of contaminated needles & syringes, and vertical
transmission from mother to child during childbirth.
Without intervention, a mother who is positive for HBsAg
confers a 20% risk of passing the infection to her offspring
at the time of birth. This risk is as high as 90% if the
mother is also positive for HBeAg.
HBV can be transmitted between family members within
households, possibly by contact of nonintact skin or mucous
membrane with secretions or saliva containing HBV.
However, at least 30% of reported hepatitis B among
adults cannot be associated with an identifiable risk factor.
Symptoms
Acute infection with hepatitis B virus
Is associated with acute viral hepatitis – an illness that
begins with general ill-health, loss of appetite, nausea,
vomiting, body aches, mild fever, dark urine, and then
progresses to development of jaundice.

It has been noted that itchy skin has been an indication as
a possible symptom of all hepatitis virus types.

The illness lasts for a few weeks and then gradually
improves in most affected people.

A few patients may have more severe liver disease
(fulminant hepatic failure), and may die as a result of it.

The infection may be entirely asymptomatic and may go
unrecognized.
Chronic infection with Hepatitis B virus
May be either asymptomatic or may be associated with a
chronic inflammation of the liver (chronic hepatitis),
leading to cirrhosis over a period of several years.



This type of infection dramatically increases the incidence
of hepatocellular carcinoma (liver cancer).
Chronic carriers are encouraged to avoid consuming
alcohol as it increases their risk for cirrhosis and liver
cancer.
Hepatitis B virus has been linked to the development of
Membranous glomerulonephritis (MGN).
Acute Hepatitis B Virus Infection with
Recovery
Typical Serologic
Course
Symptoms
HBeAg
anti-HBe
Total anti-HBc
Titr
e
0
4
anti-HBs
IgM anti-HBc
HBsAg
8
12 16 20 24 28 32 36
Weeks after Exposure
52
100
Progression to Chronic Hepatitis B Virus
Infection Typical Serologic
Acute
Chronic
Course
(6 months)
(Years)
HBeAg
anti-HBe
HBsAg
Total antiHBc
Titre
IgM antiHBc
0 4 8 12 16 20 24 28 32 36
Weeks after
52
Years
Outcome of Hepatitis B Virus
Infection
by Age at Infection
100
80
80
60
40
Chronic Infection
60
40
Chronic Infection (%)
20
20
Symptomatic Infection
0
Birth
1-6 months
7-12 months
Age at Infection
1-4 years
0
Older Children
and Adults
Symptomatic Infection (%)
Chronic Infection (%)
100
Treatment




Acute hepatitis B infection does not usually require treatment
because most adults clear the infection spontaneously.
Early antiviral treatment may only be required in fewer than
1% of patients, whose infection takes a very aggressive course
("fulminant hepatitis") or who are immunocompromised.
On the other hand, treatment of chronic infection may be
necessary to reduce the risk of cirrhosis and liver cancer.
Chronically infected individuals with persistently elevated
serum alanine aminotransferase, a marker of liver damage,
and HBV DNA levels are candidates for therapy.
Treatment



Although none of the available drugs can clear the infection, they
can stop the virus from replicating, and minimize liver damage
such as cirrhosis and liver cancer.
Currently, there are seven medications licensed for treatment of
hepatitis B infection in the United States. These include antiviral
drugs lamivudine (Epivir), adefovir (Hepsera), tenofovir (Viread),
telbivudine (Tyzeka) and entecavir (Baraclude) and the two
immune system modulators interferon alpha-2a and alfa-2a
(Pegasys).
The use of interferon, which requires injections daily or thrice
weekly, has been supplanted by long-acting pegylated interferon,
which is injected only once weekly.


The treatment works by reducing the viral
load, (the amount of virus particles as
measured in the blood), which in turn
reduces viral replication in the liver.
Infants born to mothers known to carry
hepatitis B can be treated with antibodies
to the hepatitis B virus (hepatitis B
immune globulin or HBIg). When given
with the vaccine within twelve hours of
birth, the risk of acquiring hepatitis B is
reduced 95%. This treatment allows a mother to safely breastfeed
her child.
Reactivation

Hepatitis B virus DNA persists in the body after infection
and in some people the disease re-occurs.

Although rare, reactivation is seen most often in people
with impaired immunity.

Hepatitis B goes through cycles of replication and nonreplication.

Approximately 50% of patients experience acute
reactivation.



Male patients with baseline ALT of 200 UL/L are three
times more likely to develop a reactivation than patients
with lower levels.
Patients who undergo chemotherapy are at risk for HBV
reactivation.
The current view are that immunosuppressive drugs favor
increased HBV replication while inhibiting cytotoxic T cell
function in the liver.
Prognosis

Hepatitis B virus infection may either be acute (self-limiting) or
chronic (long-standing). Persons with self-limiting infection clear
the infection spontaneously within weeks to months.

Children are less likely than adults to clear the infection.

However, only 5% of newborns that acquire the infection from
their mother at birth will clear the infection.

This population has a 40% lifetime risk of death from cirrhosis or
hepatocellular carcinoma.




Of those infected between the age of one to six, 70% will clear
the infection.
Hepatitis D infection can only occur with a concomitant infection
with Hepatitis B virus because the Hepatitis D virus uses the
Hepatitis B virus surface antigen to form a capsid.
Co-infection with hepatitis D increases the risk of liver cirrhosis
and liver cancer.
Polyarteritis nodosa is more common in people with hepatitis B
infection.
Prevention







The vaccine was originally prepared from plasma obtained from patients who
had long-standing hepatitis B virus infection.
However, currently, these are more often made using recombinant DNA
technology, though plasma-derived vaccines continue to be used; the two
types of vaccines are equally effective and safe.
Following vaccination Hepatitis B Surface antigen may be detected in serum
for several days; this is known as vaccine antigenaemia.
Vaccine is generally administered in either a two, three, or four dose
schedules; and can be received by infants to adults.
It provides protection for 85-90% of individuals, and lasts for 23 years.
Unlike Hepatitis A, Hepatitis B does not generally spread through water and
food.
Instead, it is transmitted through body fluids, from which prevention is
taken to avoid: unprotected sexual contact, blood transfusions, re-use of
contaminated needles and syringes, and vertical transmission during child
birth.
HCV



Hepatitis C is an infectious disease affecting the liver,
caused by the hepatitis C virus (HCV).
The infection is often asymptomatic, but once established,
chronic infection can progress to scarring of the liver
(fibrosis), and advanced scarring (cirrhosis).
No vaccine against hepatitis C is available. The existence of
hepatitis C (originally "non-A non-B hepatitis") was
postulated in the 1970s and proved conclusively in 1988.
History





In the mid 1970s, Harvey J. Alter, Chief of the Infectious Disease
Section in the Department of Transfusion Medicine at the National
Institutes of Health, and his research team demonstrated that most
post-transfusion hepatitis cases were not due to hepatitis A or B
viruses.
Despite this discovery, international research efforts to identify the
virus, initially called non-A, non-B hepatitis (NANBH), failed for the
next decade.
In 1987, Michael Houghton, Qui-Lim Choo, and George Kuo at Chiron
Corporation, collaborating with Dr. D.W. Bradley from CDC, utilized a
novel molecular cloning approach to identify the unknown organism.
In 1988, the virus was confirmed by Alter by verifying its presence in
a panel of NANBH specimens.
In April of 1989, the discovery of the virus, re-named hepatitis C
virus (HCV), was published in two articles in the journal Science.
Chiron filed for several patents on the virus and its diagnosis.
Virology





The Hepatitis C virus (HCV) is a small (50 nm in size), enveloped,
single-stranded, positive sense RNA virus.
It is the only known member of the hepacivirus genus in the family
Flaviviridae. There are six major genotypes of the hepatitis C virus,
which are indicated numerically (e.g., genotype 1, genotype 2,
etc.).
The hepatitis C virus (HCV) is transmitted by blood-to-blood
contact.
In developed countries, it is estimated that 90% of persons with
chronic HCV infection were infected through transfusion of
unscreened blood or blood products or via injecting drug use or,
rarely, by inhalational drug use.
In developing countries, the primary sources of HCV infection are
unsterilized injection equipment and infusion of inadequately
screened blood and blood products.
Epidemiology








Hepatitis C infects nearly 200 million people worldwide and 4 million in the
United States.
There are about 35,000 to 185,000 new cases a year in the United States,
and hepatitis C is the leading cause of liver transplant in the USA.
Co-infection with HIV is common and rates among HIV positive populations
are higher.
.
A survey conducted in California showed prevalence of up to 34% among
prison inmates; 82% of subjects diagnosed with hepatitis C have previously
been in jail, and transmission while in prison is well described.
Prevalence is higher in some countries in Africa and Asia.
Egypt has the highest seroprevalence for HCV, up to 20% in some areas.
There is a hypothesis that the high prevalence is linked to a now-discontinued
mass-treatment campaign for schistosomiasis, which is endemic in that
country.
Regardless of how the epidemic started, a high rate of HCV transmission
continues in Egypt, both iatrogenically and within the community and
household.
Co-Infection with HIV





Approximately 350,000, or 35% of patients in the
USA infected with HIV are also infected with the
hepatitis C virus, mainly because both viruses are
blood-borne and present in similar populations.
In other countries co-infection is less common,
and this is possibly related to differing drug
policies.
HCV is the leading cause of chronic liver disease
in the USA.
It has been demonstrated in clinical studies that
HIV infection causes a more rapid progression of
chronic hepatitis C to cirrhosis and liver failure.
This is not to say treatment is not an option for
those living with co-infection.
Transmission







Injection drug use
Those who currently use or have used drug injection as their delivery
route for illicit drugs are at increased risk for getting hepatitis C
because they may be sharing needles or other drug paraphernalia
(includes cookers, cotton, spoons, water, etc.), which may be
contaminated with HCV-infected blood.
An estimated 60% to 80% of all IV drug users in the United States
have been infected with HCV.
Drug use by nasal inhalation (Drugs that are "snorted")
Researchers have suggested that the transmission of HCV may be
possible through the nasal inhalation (insuffulation) of illegal drugs
such as cocaine and crystal methamphetamine when straws
(containing even trace amounts of mucus and blood) are shared
among users.
Blood products
Blood transfusion, blood products, or organ transplantation prior to
implementation of HCV screening (in the U.S., this would refer to
procedures prior to 1992) is a decreasing risk factor for hepatitis C.
Transmission Cont.







Sexual transmission of HCV is considered to be rare.
Studies show the risk of sexual transmission in heterosexual, monogamous relationships is
extremely rare or even null.
Tattooing dyes, ink pots, stylets and piercing implements can transmit HCV-infected blood from one
person to another if proper sterilization techniques are not followed. Tattoos or piercings performed
before the mid 1980s, "underground," or non-professionally are of particular concern since sterile
techniques in such settings may have been or be insufficient to prevent disease. Despite these
risks, it is rare for tattoos to be directly associated with HCV infection and the U.S.
Shared personal care items
Personal care items such as razors, toothbrushes, cuticle scissors, and other manicuring or
pedicuring equipment can easily be contaminated with blood. Sharing such items can potentially
lead to exposure to HCV. Appropriate caution should be taken regarding any medical condition
which results in bleeding such as canker sores, cold sores, and immediately after flossing.
HCV is not spread through casual contact such as hugging, kissing, or sharing eating or cooking
utensils.
Vertical transmission
Vertical transmission refers to the transmission of a communicable disease from an infected mother
to her child during the birth process.
Mother-to-child transmission of hepatitis C has been well described, but occurs relatively
infrequently. Transmission occurs only among women who are HCV RNA positive at the time of
delivery; the risk of transmission in this setting is approximately 6 out of 100.
Among women who are both HCV and HIV positive at the time of delivery, the risk of transmitting
HCV is increased to approximately 25 out of 100.
The risk of vertical transmission of HCV does not appear to be associated with method of delivery
or breastfeeding.
Signs &Symptoms








Acute
First 6 months after infection with HCV.
Between 60% to 70% of people infected develop no symptoms during the
acute phase.
In the minority of patients who experience acute phase symptoms, they
are generally mild and nonspecific, and rarely lead to a specific diagnosis
of hepatitis C.
Symptoms of acute hepatitis C infection include decreased appetite,
fatigue, abdominal pain, jaundice, itching, and flu-like symptoms.
The hepatitis C virus is usually detectable in the blood within one to three
weeks after infection, and antibodies to the virus are generally detectable
within 3 to 12 weeks.
Approximately 15-40% of persons infected with HCV clear the virus from
their bodies during the acute phase as shown by normalization in liver
function tests (LFTs) such as alanine transaminase (ALT) & aspartate
transaminase (AST) normalization, as well as plasma HCV-RNA clearance
(this is known as spontaneous viral clearance).
The remaining 60-85% of patients infected with HCV develop chronic
hepatitis C, i.e., infection lasting more than 6 months.
Previous practice was to not treat acute infections to see if the person
would spontaneously clear; recent studies have shown that treatment
during the acute phase of genotype 1 infections has a greater than 90%
success rate with half the treatment time required for chronic infections.
Chronic HCV







Hepatitis C virus persisting for more than six months.
Clinically, it is often asymptomatic and it is mostly discovered accidentally.
Recent data suggest that among untreated patients, roughly one-third progress to
liver cirrhosis in less than 20 years. Another third progress to cirrhosis within 30
years. The remainder of patients appear to progress so slowly that they are
unlikely to develop cirrhosis within their lifetimes.
Factors that have been reported to influence the rate of HCV disease progression
include age (increasing age associated with more rapid progression), gender
(males have more rapid disease progression than females), alcohol consumption
(associated with an increased rate of disease progression), HIV coinfection
(associated with a markedly increased rate of disease progression), and fatty liver
(the presence of fat in liver cells has been associated with an increased rate of
disease progression).
Symptoms specifically suggestive of liver disease are typically absent until
substantial scarring of the liver has occurred.
However, hepatitis C is a systemic disease and patients may experience a wide
spectrum of clinical manifestations ranging from an absence of symptoms to a
more symptomatic illness prior to the development of advanced liver disease.
Generalized signs and symptoms associated with chronic hepatitis C include
fatigue, marked weight loss, flu-like symptoms, muscle pain, joint pain,
intermittent low-grade fevers, itching, sleep disturbances, abdominal pain
(especially in the right upper quadrant), appetite changes, nausea, diarrhea,
dyspepsia, cognitive changes, depression, headaches, and mood swings.
Cont.


Chronic hepatitis C, more than other forms of
hepatitis, is diagnosed because of extrahepatic
manifestations associated with the presence of
HCV such as thyroiditis with hyperthyreosis or
hypothyreosis, porphyria cutanea tarda,
cryoglobulinemia (a form of small-vessel vasculitis)
and glomerulonephritis, specifically
membranoproliferative glomerulonephritis (MPGN).
Hepatitis C is also associated with sicca syndrome
(an autoimmune disorder), thrombocytopenia,
lichen planus, diabetes mellitus and with B-cell
lymphoproliferative disorders.
Diagnosis





The diagnosis of "hepatitis C" is rarely made during the acute phase of the
disease.
The diagnosis of chronic phase hepatitis C is also challenging due to the absence
or lack of specificity of symptoms until advanced liver disease develops, which
may not occur until decades into the disease.
Chronic hepatitis C may be suspected on the basis of the medical history
(particularly if there is any history of IV drug abuse or inhaled substance usage
such as cocaine), a history of piercings or tattoos, unexplained symptoms, or
abnormal liver enzymes or liver function tests found during routine blood testing.
Occasionally, hepatitis C is diagnosed as a result of targeted screening such as
blood donation (blood donors are screened for numerous blood-borne diseases
including hepatitis C) or contact tracing.
Serological blood tests used to detect antibodies to HCV. Overall, HCV antibody
tests have a strong positive predictive value for exposure to the hepatitis C virus,
but may miss patients who have not yet developed antibodies (seroconversion),
or have an insufficient level of antibodies to detect. Rarely, people infected with
HCV never develop antibodies to the virus and therefore, never test positive
using HCV antibody screening.
Because of this possibility, RNA testing (see nucleic acid testing methods below)
should be considered when antibody testing is negative but suspicion of hepatitis
C is high (e.g. because of elevated transaminases in someone with risk factors
for hepatitis C).
Diagnosis cont.




Anti-HCV antibodies indicate exposure to the virus, but cannot
determine if ongoing infection is present. All persons with positive
anti-HCV antibody tests must undergo additional testing for the
presence of the hepatitis C virus itself to determine whether
current infection is present. The presence of the virus is tested for
using molecular nucleic acid testing methods such as polymerase
chain reaction (PCR), transcription mediated amplification (TMA),
or branched DNA (b-DNA).
All HCV nucleic acid molecular tests have the capacity to detect
not only whether the virus is present, but also to measure the
amount of virus present in the blood (the HCV viral load).
The HCV viral load is an important factor in determining the
probability of response to interferon-based therapy, but does not
indicate disease severity nor the likelihood of disease progression.
In people with confirmed HCV infection, genotype testing is
generally recommended. HCV genotype testing is used to
determine the required length and potential response to
interferon-based therapy
Treatment







Current treatment is a combination of pegylated interferon alpha
(brand names Pegasys and PEG-Intron) and the antiviral drug
ribavirin for a period of 24 or 48 weeks, depending on genotype.
Indications for treatment include patients with proven hepatitis C
virus infection, Sustained cure rates (sustained viral response) of 75%
or better occur in people with genotypes HCV 2 and 3 in 24 weeks of
treatment, about 50% in those with genotype 1 with 48 weeks of
treatment and 65% for those with genotype 4 in 48 weeks of
treatment.
About 80% of hepatitis C patients in the United States have genotype
1. Genotype 4 is more common in the Middle East and Africa.
Should treatment with pegylated ribivirin-interferon not return a 2-log
viral reduction or complete clearance of RNA (termed early virological
response) after 12 weeks for genotype 1, the chance of treatment
success is less than 1%.
Early virological response is typically not tested for in non-genotype 1
patients, as the chances of attaining it are greater than 90%.
The mechanism of action is not entirely clear, because even patients
who appear to have had a sustained virological response still have
actively replicating virus in their liver and peripheral blood
mononuclear cells.
The evidence for treatment in genotype 6 disease is currently sparse,
and the evidence that exists is for 48 weeks of treatment at the same
doses as are used for genotype 1 disease.
Treatment Cont.
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Those with low initial viral loads respond much better to treatment
than those with higher viral loads (greater than 2 million virions/ml).
Current combination therapy is usually supervised by physicians in
the fields of gastroenterology, hepatology or infectious disease.
The treatment may be physically demanding, particularly for those
with a prior history of drug or alcohol abuse. It can qualify for
temporary disability in some cases.
A substantial proportion of patients will experience a panoply of side
effects ranging from a 'flu-like' syndrome (the most common,
experienced for a few days after the weekly injection of interferon) to
severe adverse events including anemia, cardiovascular events and
psychiatric problems such as suicide or suicidal ideation. The latter
are exacerbated by the general physiological stress experienced by
the patient.
Current guidelines strongly recommend that hepatitis C patients be
vaccinated for hepatitis A and B if they have not yet been exposed to
these viruses, as this would radically worsen their liver disease.
Alcoholic beverage consumption accelerates HCV associated fibrosis
and cirrhosis, and makes liver cancer more likely; insulin resistance
and metabolic syndrome may similarly worsen the hepatic prognosis.
There is also evidence that smoking increases the fibrosis (scarring)
rate.
During Pregnancy & Breast
Feeding
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If a pregnant woman has risk factors for hepatitis C, she should be tested for
antibodies against HCV.
About 4% infants born to HCV infected women become infected.
There is no treatment that can prevent this from happening.
There is a high chance of the baby ridding the HCV in the first 12 months.
In a mother that also has HIV, the rate of transmission can be as high as 19%.
There are currently no data to determine whether antiviral therapy reduces
perinatal transmission.
Ribavirin and interferons are contraindicated during pregnancy. However,
avoiding fetal scalp monitoring and prolonged labor after rupture of
membranes may reduce the risk of transmission to the infant.
HCV antibodies from the mother may persist in infants until 15 months of age.
If an early diagnosis is desired, testing for HCV RNA can be performed between
the ages of 2 and 6 months, with a repeat test done independent of the first
test result.
If a later diagnosis is preferred, an anti-HCV test can performed after 15
months of age.
Most infants infected with HCV at the time of birth have no symptoms and do
well during childhood.
There is no evidence that breast-feeding spreads HCV. To be cautious, an
infected mother should avoid breastfeeding if her nipples are cracked and
bleeding.
Alternative Therapy
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Several alternative therapies purport to
maintain liver functionality, rather than
treat the virus itself, thereby slowing the
course of the disease to retain quality of
life.
As an example, extract of Silybum
marianum and Sho-saiko-to are sold for
their HCV related effects; the first is said
to provide some generic help to hepatic
functions, and the second claims to aid in
liver health and provide some antiviral
effects.[25]
Prevention
The following guidelines will prevent infection with the hepatitis C
virus, which is spread by blood:
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Avoid sharing drug needles or any other drug paraphernalia
including works for injection or bills or straws
Avoid unsanitary tattoo methods
Avoid unsanitary body piercing methods
Avoid unsanitary acupuncture
Avoid needlestick injury
Avoid sharing personal items such as toothbrushes, razors, and
nail clippers.
Use latex condoms correctly and every time if not in a long-term
monogamous relationship
Proponents of harm reduction believe that strategies such as the
provision of new needles and syringes, and education about safer
drug injection procedures, greatly decreases the risk of hepatitis C
spreading between injecting drug users.
No vaccine protects against contracting hepatitis C, or helps to
treat it. Vaccines are under development and some have shown
encouraging results.